T-cell exhaustion is described as a state of T cell dysfunction resulting in the increase of inhibitory receptors (PD-1, CD244, CD160, LAG-3, TIM-3) with poor effector function (hyperproliferation, diminished cytotoxicity, reduced cytokine generation), and progressive loss of T cell function in cases with AML [134]. This evidence concerns the gene PDCD1 and acute myeloid leukemia.